AAO READING

RETINA

MACULAR HOLE
 INTRODUCTION
• A FULL-THICKNESS DEPLETION OF THE NEURAL RETINAL TISSUE IN THE
CENTRE OF MACULA
• MOST COMMONLY UNILATERAL
• MOST OF THEM CAUSED BY IDIOPATHIC
 ETIOLOGY
• COMMON CAUSE
– HIGH MYOPIA
– IDIOPATHIC
– TRAUMA

• OTHER CAUSE
– CYSTOID MACULAR EDEM
– PDR
– HIPERTENSIVE RETINOPATHY
– COROIDAL NEOVASCULARISATION
 CLASSIFICATION
• PRIMERY MH
– COMMONLY AN IDIOPATHIC CAUSED BY VITREOUS
TRACTION ON THE FOVEAL
• SECONDARY MH
– CAUSED BY OTHER PATHOLOGIES NOT ASSOCIATED
WITH VITREOMACULAR TRACTION, SUCH AS BLUNT
TRAUMA, HIGH MYOPIA, MACULAR TELANGIECTASIA,
MACULAR OEDEMA
 PATHOGENESIS
 TRAUMATIC THEORY
DIRECT OR INDIRECT OCULAR TRAUMA
TRAUMA CAUSES IMMEDIATE MAULAR HOLE
FORMATION FROM MECHANICAL ENERGY CREATED BY
VITREOUS FLUID WAVES AND COUNTERCOUP
MACULAR NECROSIS OR LASERATION
MORE COMMON IN YOUNG BOYS
 PATHOGENESIS
• CYSTOID DEGENERATION
THEORY
– CYSTIC DEGENERATION OF
THE CENTER OF THE
MACULA
– DUE TO : HT, RETINAL
VESSEL OCLUSION,
TRAUMA
– CYST COALESCENCE  MH
 PATHOGENESIS
• VITREOUS THEORY
ANTERO-POSTERIOR VITREOUS BAND 
MACULAR TRACTION 
MACULAR CYSTOID DEGENERATION 
MACULAR HOLE
 PATHOGENESIS
• CURRENT THEORY
POSTERIOR HYALOID APPLIES TRACTION TO THE
FOVEOLA/UMBO AND CAUSES IT TO STRETCH 
UMBO DEHISCES BECAUSE IT IS THE THINNEST
POINT IN THE FOVEA  MIDDLE AND INNER RETINA
ABSORBS VITREOUS FLUID AT THE EXPOSED EDGES
OF THE HOLE AND BEGINS TO SWELL
HOLE ENLARGES BECAUSE OF A LATERAL EXTENSIO OF
FLUID INTO THE OUTER PLEXIFORM LAYER  INNER
RETINA IS BRACHED  DUE TO THE HYDRATION OF TE
FOVEA AND PERIFOVEAL MACULA, THE MACULAR HOLE
PROGRESSES
 ROLE OF ILM
• SCAFFOLD FOR PROLIFERATION OF CELLULAR
COMPONENTS LIKE MYOFIBROBLASTS, FIBROCYTES,
RPE CELLS, FIBROUS ASTROCYTS  CAUSING
TANGENTIAL TRACTION AROUND FOVEA  FTMH
FORMATION  MAY ALSO CONTRIBUTE TO
ENLARGEMENT OF MH
 STADIUM MH
• A stage 0, or premacular, hole occurs when a PVD
with persistent foveal attachment develops. Subtle
loss of the foveal depression can be observed, and
visual acuity is usually unaffected. Most stage 0 holes
do not progress to advanced stages.
• A stage 1 macular hole (impending macular hole) typically causes visual symptoms
of metamorphopsia and central vision decline, usually to a visual acuity range of
20/25 to 20/60.
• The characteristic findings are either a small yellow spot (stage 1A) or a yellow circle
(stage 1B) in the fovea.
• OCT examination reveals that a stage 1A hole is a foveal “pseudocyst,” or horizontal
splitting (schisis), associated with vitreous traction to the foveal center.
• A stage 1B hole indicates a break in the outer fovea, the margins of which constitute
the yellow ring noted clinically. Spontaneous resolution of a stage 1 hole occurs in
approximately 50% of cases without ERM. This stage represents VMT syndrome.
• A stage 2 macular hole represents an early full-thickness macular hole
that is less than 400 μm in diameter. It results from the progression of
a foveal schisis (pseudocyst) to a fullthickness dehiscence, as a
tractional break develops in the “roof” (inner layer) of the pseudocyst.
• Progression to stage 2 is accompanied by a further decline in visual
acuity. OCT demonstrates the full-thickness defect and the continuing
attachment of the posterior hyaloid to the foveal center.
• This stage represents VMT syndrome with a small- to medium-sized
macular hole.
• A stage 3 macular hole is a fully developed hole (≥400
μm in diameter), typically surrounded by a rim of
thickened and detached retina. Visual acuity ranges
widely.
• The posterior hyaloid remains attached to the optic
nerve head but is detached from the fovea.
• On OCT, this stage represents a large macular hole with
no VMT (Activity 17-3, Fig 17-8).
• A stage 4 macular hole is a fully developed hole with
a complete posterior vitreous detachment, as
evidenced by the presence of a Weiss ring.
• On OCT, this stage represents a large macular hole
with no VMT.
 MANAGEMENT
• Stage 1 macular holes have an approximate 50% rate of spontaneous
resolution and thus are typically monitored.
• An alternative management option for stage 1 holes or holes that are
less than 250 μm in diameter is the intravitreal injection of ocriplasmin.
• In the ocriplasmin phase 3 clinical trial, the closure rate of full-thickness
macular holes was 40.6% overall and 58.3% for holes of less than 250
μm diameter.
• Ocriplasmin is most effective in eyes with focal adhesions and much less
effective for broad vitreoretinal adhesions or adhesions associated with
an ERM.
• For stage 2 or greater macular holes, surgical intervention is
recommended—specically, pars plana vitrectomy with gas
tamponade; in most recent case series, the success rate of this
procedure for closure and vision improvement was greater than
90% (see Chapter 20 in this volume).
• Modications of routine macular hole surgery are usually reserved
for very large, chronic, or nonclosing holes; these include inverted
ILM aps and autologous retinal grafts composed of peripheral
retina. Although these techniques may achieve anatomical hole
closure, visual acuity may not improve.
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